Hepatic Vitamin A Uptake Storage and Release

Once chylomicra enter lymph and plasma, chylomi-cron remnants are formed rapidly by lipolysis. The majority of chylomicron remnants, still containing vitamin A, are quickly cleared into liver parenchy-mal cells (hepatocytes) by receptor-mediated endo-cytosis. Adipose and other tissues, including the mammary glands during lactation, also take up small amounts of newly absorbed vitamin A during the lipolysis of chylomicra. Within a few hours of chylomicron remnant clearance by hepatocytes, most of these newly absorbed retinyl esters are hydrolyzed and the retinol component is re-esterified, forming new retinyl esters. Newly formed retinyl palmitate and stearate are deposited in lipid droplets in vitamin A-storing stellate cells. In the vitamin A adequate state, more than 90% of total body vitamin A is stored in liver stellate cells. Small numbers of similar stellate cells have been described in extrahepatic tissues, suggesting the presence of a network of vitamin A-storing cells throughout the body.

As retinol is needed, stellate cell retinyl esters are hydrolyzed by one or more REHs and retinol is transferred back to hepatocytes for combination with newly synthesized RBP. The holo-RBP complex then passes through the Golgi secretory apparatus and binds noncovalently with a tetramer of TTR. The larger size of this transport complex (~75kDa) compared to holo-RBP alone (~21 kDa) helps to prevent the rapid loss of retinol and RBP during renal glomerular filtration.

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